Panangin forte 60 pcs. film-coated tablets

Pharmacology

Panangin is an important source of microelements. The medication helps maintain electrolyte balance. Involved in the metabolic process, has an antiarrhythmic effect.

Potassium is responsible for the normal functioning of the heart, conducting nerve impulses along the fibers. With a lack of this substance, there is excitability of nerves and tissues. With a small amount of potassium, the coronary arteries dilate, and with a large dosage, a narrowing of the lumen is observed.

Magnesium is necessary for processes associated with the intake and expenditure of energy. The trace element is present in the pentose phosphate structure of DNA and is involved in the process of cell division and growth, and RNA synthesis. Magnesium is a natural blocker of slow calcium channels and prevents the release of free fatty acids.

The medicine is well absorbed. Exits through the kidneys.

Panangin in the treatment and prevention of cardiovascular diseases

It has now been established (data from the Framingham Study) that 12% of all natural deaths occur due to sudden death. In 70% of cases, the cause of sudden cardiac death is severe hemodynamic disturbances in the pumping activity of the heart, caused by developed electrophysiological changes in the rhythm of cardiac activity - arrhythmogenic death due to intracellular electrolyte imbalance (“potassium and magnesium deficiency”) [3]. Thus, it has been proven that potassium and magnesium ions in the blood plasma play an important role in maintaining the elasticity of the vascular wall and maintaining its normal functioning [4]. In 1998, three American scientists - F. Furchgott, L. Ignarro and F. Murad - were awarded the Nobel Prize in Physiology or Medicine for their discovery of the role of nitric oxide (NO) as a signaling molecule in the cardiovascular system. Modern ideas about the regulation of vascular tone are that in response to all irritating stimuli, the artery reacts in the same way - by increasing the tone of muscle fibers and narrowing (spasm). However, the cells of the inner lining of the arteries, the endothelium, produce NO, which relaxes these muscle fibers, leading to the expansion of the lumen of the vessel [5]. With age, as well as in smokers (not only active, but also passive), in people with obesity, arterial hypertension (AH), and others, some endothelial abilities, including the secretion of NO, are lost, and a condition called “endothelial dysfunction” develops. . Endothelial dysfunction is characterized by a decrease in the elasticity of the vascular wall and is a significant factor leading to increased blood pressure (BP) and the development of atherosclerosis and a number of CVDs. As the results of studies by domestic and foreign authors have shown, potassium and magnesium prevent the development of endothelial dysfunction and the formation of hypertension [6]. Potassium and magnesium in ionized form are positive ions - cations, respectively, with one (K+) and double positive charges (Mg2+); are among the most abundant elements on Earth. There is especially a lot of potassium and magnesium in the water of the World Ocean, which in its electrolyte composition is close to the electrolyte composition of blood serum. Potassium is the main intracellular cation in tissues of various organs. Under normal conditions, its content in the cell is 150–160 mmol/l, and in the blood serum – 3.5–5.5 mmol/l. Potassium ions (K+) are involved in the formation of cellular action potentials (depolarization and repolarization phases), transmission of nerve impulses, contraction of cardiomyocytes, skeletal and smooth muscle fibers, and regulate and maintain the functions of the urinary system. Under normal conditions, potassium comes from food and is absorbed through the gastrointestinal tract, followed by excretion of excess through the kidneys. The daily potassium requirement of an adult is 40–100 mmol/l [9]. With hypokalemia, the symptoms are associated with the cardiovascular system - due to the fact that the heart is more susceptible to diseases caused by potassium deficiency. On the part of the cardiovascular system, metabolic disorders and functional insufficiency of the myocardium, arrhythmia, tachycardia, deafness of heart sounds, the occurrence of heart attacks, heart failure, and low blood pressure are observed. Among the cations present in the human body, magnesium (Mg2+) ranks 4th in concentration, and in the cell it ranks 2nd after K+. Under normal conditions, the concentration of Mg2+ in blood serum is 0.65–1.1 mmol/l, in erythrocytes – 1.65–2.55 mmol/l. The daily requirement of an adult for magnesium is 25–35 mmol/l [10]. Magnesium is a universal regulator of biochemical and physiological processes: it is involved in energy, plastic and electrolyte metabolism. These are carbohydrate and energy processes, immune status, contraction of smooth muscle cells in general and cardiomycytes in particular, mineral and cholesterol metabolism, regulation of detoxification metabolism in the liver. In recent years, the important role of this ion in protein and cholesterol metabolism has been noted; the role of magnesium as a regulator of cell growth and normalization of purine metabolism (hypoxia/hypoergosis) has been revealed. Mg2+ is very important for the normal functioning of myocardial cells and the central nervous system, because takes part in receptor formations, preserves the processes of oxidative phosphorylation in mitochondria for the formation of ATP and adequate functioning of transmembrane ion transport. Playing the role of a natural calcium antagonist, magnesium is involved in the relaxation of muscle fiber, reduces platelet aggregation ability, and maintains normal transmembrane potential in electrically excitable tissues. Magnesium affects the endothelium, which plays a key role in vascular homeostasis through the production of nitric oxide and participation in the control of platelet aggregation. It has been proven that hypomagnesemia increases the activity of thromboxane A2, which is accompanied by damage to the vascular endothelium. One multicenter study showed that long-term Mg2+ therapy led to significant endothelium-dependent dilatation. Moreover, in relation to hypertension and coronary heart disease, a connection was also previously established with the serum concentration of magnesium, and not with its consumption [11]. Clinical manifestations of magnesium deficiency are increased heart rate, diastolic blood pressure, sleep disturbance, increased excitability, chronic fatigue syndrome. A low concentration of magnesium in red blood cells is combined with increased blood pressure at rest and during stress, as well as with spasm of the coronary arteries. On the ECG, magnesium deficiency is manifested by slowing of atrioventricular conduction, widening of the QRS complex, prolongation of the QT interval, nonspecific decrease in the ST interval, flattening of the T wave and the formation of a pronounced U wave. The appearance of potassium-magnesium deficiency is also often expressed in the occurrence of treatment-resistant cardiac arrhythmias, This is especially true for patients with acute inflammatory processes in the myocardium and with various manifestations of acute coronary insufficiency, ECG changes in the form of prolongation of the QT interval, ventricular extrasystoles, tachycardia topsаdes de pointes, sometimes atrial fibrillation, early cardiotoxicity of digitalis drugs. It has been proven that in the elderly, magnesium deficiency leads to the development of atherosclerosis and correlates with age (this is due to age-related metabolic characteristics). These facts explain the slowdown in atherosclerotic processes and mortality from myocardial infarction (MI) in residents of areas with a high content of magnesium salts in water. The consequence of potassium-magnesium deficiency quite often is cardiac rhythm disturbances, in particular the development of atrial fibrillation [12,13], which is most often associated with coronary artery disease, chronic heart failure (CHF), and hypertension. In 60% of patients with atrial fibrillation, hypertension is detected, which in most cases is a concomitant disease. Atrial fibrillation in 25–40% of cases can be a complication of invasive interventions for coronary artery disease (percutaneous coronary angioplasty) due to magnesium and potassium deficiency [14]. Treatment. Therapy of seriously ill and critically ill patients with K+ and Mg2+ has been known for quite a long time. The important role of these cations in the pathogenesis of stress and its treatment was shown by G. Selye (1930) and at the same time proposed a prototype of a polarizing mixture. In 1960, D. SodiPollares, in a small non-randomized study, showed that the use of a glucose-insulin-potassium (GIK) mixture improved early survival of patients with acute forms of coronary artery disease. This was also confirmed by later prospective randomized studies ECLA [15] and DIGAMI [16], which noted a significant reduction in the mortality rate in patients who had suffered an MI with the introduction of GIK. The polarizing mixture proposed by H. Laborit, or more precisely repolarizing (glucose-potassium-magnesium-insulin), was created taking into account the effect of switching the metabolism of a hypoxically damaged organ (myocardium) or body from the wasteful oxidation of free fatty acids to glucose, which is more energetically favorable under hypoxic conditions. This allows, under conditions of hypoxia/ischemia, to prevent the development of catecholamine myocardial micronecrosis and rhythm disturbances, including fatal ones. According to a number of authors, such treatment can reduce the mortality rate of patients with acute myocardial infarction (AMI) by 15–20%, depending on the composition and time of administration of the specified mixture. Riker (1990) proposed the use of a hyperpolarizing mixture for cardiogenic shock: concentrated glucose (500 ml), large doses of potassium and insulin. The author associates a decrease in mortality and a pronounced antiarrhythmic effect with an improvement in the metabolism of cardiomyocytes, especially in conditions of ischemia. Glucose-insulin potassium-magnesium mixture (GIKMS) is a nonspecific modulator of myocardial metabolism that helps increase glucose uptake and oxidation. It has been established that the disturbance of local myocardial contractility, which is interpreted as hibernating myocardium, disappears with the introduction of GIMS. From these positions, the use of a polarizing mixture in the treatment of severe heart failure is important and promising [E.V. Shlyakhto, 2003]. Renowned cardiologist L. Ali said: “The heart is more than a pump. It is also an organ that requires energy provided by metabolic processes. Metabolic disease – ischemia should ideally be treated metabolically.” A meta-analysis of 19 studies (including 586 people, 412 of them with hypertension) showed a relationship between the severity of the hypotensive effect and the duration of potassium supplementation. An average reduction in blood pressure of 5.9/3.4 mmHg was demonstrated. when using tableted potassium preparations [7]. During long-term observation (on average 6.7 years) of 7563 patients with hypertension, of which 1679 received diuretics, it was noted that the resulting hypokalemia (potassium concentration less than 3.5 mmol/l) was accompanied by an increase in the incidence of cardiovascular complications [8]. It is advisable to assess changes in the concentration of potassium in the blood in parallel with the quantitative assessment of magnesium indicators, because it promotes the absorption of potassium and ensures its optimal intracellular level. Combined potassium and magnesium deficiency can lead to hypokalemia that is resistant to treatment if magnesium deficiency is not simultaneously corrected [10]. According to Shechter M. et al., the use of oral magnesium and potassium supplements in patients with coronary artery disease led to a significant increase in endothelium-dependent dilatation of the brachial artery by 15.5% (p<0.01) compared with placebo (by 4.4%, ( p>0.05)), while a linear correlation was revealed between the intracellular concentration of magnesium and the degree of vasodilation [17]. It has been established that, taking into account the antiatherogenic effects of magnesium preparations, correction of its deficiency can help slow the progression of coronary artery disease. In the ARIC (The Atherosclerosis Risk in Communities) study, after 4–7 years of follow-up of 13,922 patients, an analysis of risk factors showed an association between the development of coronary artery disease and hypomagnesemia [18]. The most pronounced magnesium deficiency occurs in patients with elevated levels of atherogenic lipids [19]. A frequent companion of patients with CVD is type 2 diabetes mellitus (DM), in which magnesium deficiency increases, especially in old age. The use of magnesium supplements in such patients improves insulin-dependent glucose utilization [20]. Potassium and magnesium deficiency in patients with CHF is associated with poor quality of life and prognosis [21]. The prescription of magnesium- and potassium-containing drugs is especially justified during long-term use of cardiac glycosides and diuretics, which provoke hypomagnesemia/hypokalemia and subsequent cardiac arrhythmias associated with a deficiency of these electrolytes [21]. The antiarrhythmic effect of magnesium occurs through its effect on the transport of sodium, potassium and calcium ions involved in the formation of the action potential [21]. As an antiarrhythmic, magnesium salts are most often used for ventricular arrhythmias (torsades de pointes) due to their ability to inhibit the development of trace depolarizations, shortening the duration of the QT interval. Magnesium can be used both for congenital long QT syndrome and for its iatrogenic variant caused by the use of class 1 antirhythmics and other drugs [22,23]. Magnesium preparations help prevent arrhythmias provoked by digitalis intoxication, when the function of the potassium-sodium pump is impaired [24]. There are many forms of drugs that can simultaneously eliminate intracellular K+ and Mg2+ deficiency. Among them, K-Mg-nicotinate, K-Mg-citrate, K-Mg-glutamate, etc. should be noted. But the most effective drug was one containing aspartic acid (K-Mg-aspartate), Panangin (), which has an optimal cost/effectiveness ratio. Aspartic acid, as an endogenous amino acid, belongs to the metabolically active glucoplastic amino acids. Due to its special affinity, it penetrates the cell and participates in intermediate metabolism. Aspartic acid is often called an electrolyte transporter. Its combination with potassium and magnesium was proposed in the 1930s. G. Selye for the treatment and prevention of emerging ischemic, hypoxic and necrotic processes in the human body. In particular, he noted the importance and effectiveness of such treatment when MI occurs. In the 1950s fundamental clinical works by H. Laborit appeared on the high effectiveness of K-Mg salt of aspartic acid in AMI, hypoxia/ischemia, conditions accompanied by the accumulation of ammonia and under-oxidized metabolic products in the body. These works show that aspartic acid, when included in the Krebs cycle, normalizes the disturbed ratios of tricarboxylic acids, actively participates in the synthesis of ATP, promotes the entry of K+ and Mg2+ into the cell and restores the adequate functioning of ion pumps under conditions of hypoxia/hypoergosis. Aspartic acid is an aliphatic amino acid present in the body as part of proteins, and in its free form plays an important role in the metabolism of nitrogenous substances and participates in the formation of pyrimidine bases and urea. By reducing the ammonia content, aspartate protects the central nervous system, normalizes the processes of excitation and inhibition in it, and stimulates the immune system. Aspartic acid promotes the conversion of carbohydrates into glucose with an increase in glycogen reserves, which is important for nutritional support in order to ensure protein-energy homeostasis. Salts of aspartic acid increase endurance and the body’s resistance to various influences, i.e. have an adaptation effect [2]. Thus, there is no doubt that at present, potassium and magnesium deficiency largely determines the pathogenetic features of many CVDs, as a result of which the use of combination drugs containing both magnesium and potassium is the basis for both the prevention and treatment of CVDs. Since 1960, the active use of K-Mg-aspartate in clinical practice began. One of the most famous preparations of K-Mg-aspartate is the drug Panangin. The positive effect of the administration of K-Mg-aspartate was shown in patients with AMI who, for one reason or another, were contraindicated for thrombolysis or angioplasty. The optimal time to start administration is the first 6 hours from the onset of the disease. Thus, T. Ryan et al. (1999) consider it advisable to administer K-Mg-aspartate in the treatment of ventricular tachycardia of the “pirouette” type, especially in patients with a prolonged QT interval, as well as prescribing this drug to patients with AMI at high risk of an unfavorable outcome. It is noted that the use of Panangin (K-Mg-aspartate) increases the effectiveness of the treatment of heart failure - metabolic and antihypoxic effects (the dose of the administered drug can be increased to 20-30 ml/day). The role of Panangin in the treatment and prevention of reperfusion arrhythmias, which are also based on hypoxia/hypoergosis and hyperoxia, is also important. The same reperfusion processes lead to the spread of the zone of myocardial damage, the occurrence of anginal attacks, and the “refreshment” of myocardial infarction – its relapses. Conducted multicenter studies indicate the effectiveness of K-Mg-aspartate in preventing these complications and reducing mortality in acute coronary syndrome. The role of Panangin is no less important for stabilizing electrolyte homeostasis in patients taking diuretics, which sometimes lead to minor quantitative changes in the composition of electrolytes, and this aggravates the course of one or another pathology underlying heart failure. Many concomitant severe diseases in patients with pathologies of the cardiovascular system also require the inclusion of K+ and Mg2+ drugs in therapy. Combination therapy for these conditions with the inclusion, if possible, of K-Mg-aspartate in solution or panangin will improve the clinical condition of patients and accelerate its stabilization. Thus, the indications for the use of K - Mg - asparaginate (Panangin) for therapeutic and preventive purposes are violation of the rhythm of cardiac activity (atrial fibrillation, ventricular arrhythmias), heart failure, metabolic syndrome (obesity, hypertension, violation of glucose tolerance, diabetes 2nd type) (as part of complex therapy) [24–26]. Contraindications for oral administration and intravenous administration are acute and chronic renal failure, oliguria, anuria, Addison's disease, atrioventricular blockade of II and III degree, cardiogenic shock (AD <90 mm Hg), hyperkalemia, hypermagnia, increased sensitivity to the components of the drug . For oral administration, severe miastenia, atrioventricular blockade of the 1st degree, hemolysis, amino acid metabolism, acute metabolic acidosis, dehydration of the body are also contraindications. Drug interactions. With the simultaneous use of Panangin with potassium -saving diuretics (triamteren, spironolactone), β -adreno -shields, cyclosporine, heparin, ACE inhibitors, NSAIDs, the risk of developing hyperkalemia up to the onset of arrhythmia and asystole. The use of potassium preparations, together with glucocorticosteroids, eliminates the hypokalemia they caused. Under the influence of potassium, there is a decrease in undesirable effects of heart glycosides. The drug enhances the negative dromo and battleship of antiarrhythmic drugs. Magnesium, which is part of Panangin, reduces the effectiveness of Neomycin, polymixin B, tetracycline and streptomycin. Anesthetics enhance the inhibitory effect of magnesium on the central nervous system. When used with dexametonium, suxaetonium, an increase in neuromuscular blockade is possible [26,27]. In the treatment of rhythm of cardiac activity, Panangins are prescribed 2-3 tablets of 3 r./Day, the maximum daily dose - 3 tablets of 3 r/day. As a maintenance or preventive therapy (to prevent the development of arrhythmias during treatment with diuretics), the drug should be prescribed 1-2 tablets 3 times a day. After eating, because The acidic medium of the contents of the stomach reduces the efficiency of the suction of panangin. The use of infusion solutions is possible with the risk of arrhythmias, as well as for their relief, for example, in patients with heart failure when taking heart glycosides. Thus, the widespread use of the Panangin drug, which simultaneously containing potassium and magnesium, which has well established itself in the complex therapy of the SSZ, has proven effectiveness in their treatment and prevention, as well as the optimal ratio of cost/efficiency, is justified. The advantages of Panangin also include over -the -counter vacation (for a tablet form). In addition, the good recognition of the drug is important with cardiologists and therapists of outpatient and stationary links. Literature 1. Kryukov N.N., Kachkovsky M.A. Therapist's reference book. Rostov -on -Don: Phoenix, 2011. 446 p. 2. Kosarev V.V., Babanov S.A. Clinical pharmacology of drugs used for cardiovascular diseases. Samara: etching, 2010. 140 p. 3. Mendis S. The Contribution of the Framingham Heart Study to the Prevention of Cardiovascular Disease: A Global Perspective // ​​Prog Cardiovasc Dis. 2010. Vol. 53 (1). R. 10-14. 4. Fox Ch, Mahoney Mc, Ramsoomar D., Carter Ca Magnesium Deficiency in African - Mericans: Does Itstribute to Increased Cardiovascular Risk Factors? // J Natl Med Assoc 2003. Vol. 95 (4). R. 257–262. 5. Kaiser L, Sparks HV. Jr. Endothelial Cells. Not Just a Cellophane Wrapper // Arch Intern Med. 1987. Vol. 147. R. 569–573. 6. Taddei S., Mattei P., Virdis A. et al. Effect of Potassium on Vasodilation to Acetylcholine in Essential Hypertension // Hypertension. 1994. Vol. 23. R. 485–490. 7. Cappucio F., McGregor G. Does Potassium Supplementation Lower Blood Pressure? A meta - ANALYSIS of Published trials // J Hypertens. 1991. Vol. 9. R. 456–473. 8. Cohen HW, Madhawan S., Alderman Mh High and Low Serum Potassium Associated with Cardiovascular Events - Treated Patients // J Hypertens. 2001. Vol. 19 (7). R. 1315–1323. 9. Peacock JM, Folsom Ar, Arnett DK et al. Relationship of Serum and Dietary Magnesium to Incident Hypertension: The atherosclerosis Risk in Communities (Aric) Study // Ann Epidemiol. 1999. Vol. 9(3). R. 159–165. 10. Avtsyn A.P., Zhavoronkov A.A., Rish M.A., Strogova L.S. Human microelentoses: etiology, classification, organopathology. M.: Medicine, 1991. 496 p. 11. Amighi J., Sabeti S., Schlager O. et al. Low Serum Magnesium Predicts Neurological Events in Patients with Advanced Atherosclerosis // Stroke. 2004. Vol. 35 (1). R. 22–27. 12. Altura BM, Shah NC, Jiang XC et al. Magnesium Deficiency Upregulates Serine Palmitoyl Transferase (SPN 1 and SPT 2) In Cardiovascular Tissues: Relationship to Serum Ionized Mg and Cytochrome C // Am J Phyysiol Heort C IRC Physiol. 2010. Vol. 299 (3). R. 932–939. 13. CHAKRABORBORTI S., Chakraborti T., Mandal M. et al. Protective Role of Magnesium in Cardiovascular Disease: A Review // Mol Cell Biochem. 2002. Vol. 238. R. 163–179. 14. Piper SN, KISSLING AH, SUTTner SW et al. Prevention of Atrial Fibrillance After Coronary Bypass Graft Surgery Assium - Magnesium - ASPARTETETETETE SOLUTION (Inzolen) // Thorac Cardiovasc Surg. 2007. Vol. 55 (7). R. 418–423. 15. Diaz R., Paolasso E., Piegas L. et al. METABOLIC MODULATION OF ACUTE MyCardial Infarction: The Ecla (Estudios Cardiologics Latinoamerica) Collaboative Group // Circulation. 1998. Vol. 98. No. 21. P. 2227–2234. 16. Hess Ml, Okabe E., Poland J. et al. Glucose, Insulin, Potassium Protection During the Course of Hyporamic Global Ischemia and Repurfusion: A New Proposed Mechanism by the Scavenging of Free Radicals // J. Cardi OVASC. Pharmacol. - 1983. - Vol. 5, No. 1. - P. 35–43. 17. Shechter M., Sharir M., Labrador Mj et al. Oral Magnesium Therapy Imprings Endothelial Function in Patients with Coronary Artery Disease // Circulation. 2000. Vol. 102 (19). R. 2353–2358. 18. Liao F., Folsom Ar, Brancati FL Is Low Magnesium Concentration a Risk Factor For Coronary Heart Disease? The atherosclerosis risk in communates (Aric) Study // Am Heart J. 1998. Vol. 136 (3). R. 480–490. 19. Ueshima K. Magnesium and Ischemic Heart Disease: A Review of Epidemiological, Experimental, and Clinical Evidences // Magnes Res. 2005. Vol. 18 (4). R. 275–284. 20. Lima MDE L., Cruz T., Rodrigues le et al. Serum and Intracelllar Magnesium Deficiency in Paty Metabolic Syndrome - Evidences for ITS Relation Resistance // Diabetes Res Clin Pract. 2009. Vol. 83 (2). R. 257–262. 21. Sueta Ca, Clarke SW, Dunlap SH Effect of Acute Magnesium Administration on the Frequency of Ventricular Arrhythmia in Paty Heart Failure // Circulation. 1994. Vol. 89. R. 660–666. 22. Banai S., Schuger C. Magnesium Sulfate Is the Treatment for Torsades de Pointes if the Right Dose Is Given // Am J Cardiol. 1990. Vol. 15. 65 (3). R. 266. 23. Zehender M., Meinertz T., Just H. Magnesium Deficiency and Magnesium Substition. Effect on Ventricular Cardiac Arrhythmias of Various Etiology // Herz. 1997. Vol. 22. SUPPL 1. R. 56–62. 24. Captured S.V., Gayvoronskaya V.V., Kulikov A.N., Schulenin S.N. Clinical pharmacology. Selected lectures. M.: GEOTAR - Media, 2009. 608 p. 25. Verbova A.F. Metabolic syndrome. Scientific and practical manual. Samara: Volga -Business, 2010. 98 p. 26. Kosarev V.V., Babanov S.A. Clinical pharmacology and rational pharmacotherapy. M.: University textbook. Infra - M, 2012. 252 p. 27. Schukin Yu.V., Ryabov A.E. Chronic coronary heart disease in old and senile age. A manual for doctors. Samara: Volga -Business, 2008. 44 p.

How to use

Pills

The medicine in tablet form is intended for oral administration. You can take 2 tablets three times a day. For maintenance purposes, you can take 1 tablet three times a day. The treatment course is 20-25 days.

In special cases, an additional therapeutic course may be required.

Intravenous administration

Panangin in the form of a solution should be administered intravenously slowly, drip-wise. The rate of administration of the drug should not be more than 25 drops per minute. This procedure can be carried out no more than 2 times a day. No more than 300 ml can be administered at a time. The dosage of the medicine for pregnant women does not require adjustment and is carried out according to the standard scheme.

For prevention purposes

Patients are often interested in questions regarding the benefits and harms of a drug. It is worth understanding that Panangin can cause many negative reactions, so you should not use it for preventive purposes. This is explained by the fact that taking medications will cause the body to become accustomed to a certain content of microelements or may lead to an excess of these microelements in the human body, which will entail many negative consequences.

Adverse reactions

The drug may cause the following side effects:

• the appearance of ulcers in the stomach;
• diarrhea;
• pain in the epigastric region;
• hemorrhage from the stomach, intestines;
• nausea, vomiting;
• feeling of dryness in the mouth;
• skin irritations;
• dizziness;
• excessive sweating.

With rapid intravenous infusion, an excessive increase in the amount of trace elements in the blood occurs.

Overdose

It is not recommended to exceed the prescribed dose. An overdose of the drug is possible, manifested by the following symptoms:

• excessive levels of potassium and magnesium ions in the blood;
• muscle hypotonicity;
• problems with the functioning of the heart, even to the point of cardiac arrest;
• arrhythmia;
• changes on the electrodiogram.

If such signs appear, you should immediately inject a solution of dextrose and sodium chloride intravenously. Depending on the patient's condition, peritoneal dialysis may be required.

Panangin forte (tab.pl/vol. 316mg+280mg No. 60)

A country

Hungary
The country of production may vary depending on the batch of goods. Please check with the operator for detailed information when confirming your order.

Active substance

Potassium and magnesium aspartate

Compound

For 1 tab. — potassium aspartate 316 mg; — in the form of potassium aspartate hemihydrate 332.6 mg; — magnesium aspartate 280 mg; - in the form of magnesium aspartate tetrahydrate 350 mg; Excipients: corn starch - 172.2 mg, talc - 20 mg, magnesium stearate - 8 mg, potato starch - 6.6 mg, povidone K30 - 6.6 mg, colloidal silicon dioxide - 4 mg. Film composition shells: talc - 7.3 mg, butyl methacrylate copolymer - 6 mg, titanium dioxide (color index: CI 77891, E171) - 5.3 mg, macrogol 6000 - 1.4 mg.

pharmachologic effect

The most important intracellular cations potassium and magnesium play a key role in the functioning of many enzymes, in the formation of bonds between macromolecules and intracellular structures and in the mechanism of muscle contractility. The intra- and extracellular ratio of potassium, magnesium, calcium and sodium ions affects myocardial contractility. Endogenous aspartate acts as a conductor of ions: it has a high affinity for cells, due to the slight dissociation of its salts, ions in the form of complex compounds penetrate into the cell. Potassium and magnesium aspartate improves myocardial metabolism. A lack of potassium and/or magnesium ions predisposes to the development of arterial hypertension, atherosclerosis of the coronary arteries and the occurrence of metabolic changes in the myocardium.

Indications for use

To eliminate potassium and magnesium deficiency as an adjunct: - for various manifestations of coronary artery disease, including acute myocardial infarction; - for chronic heart failure; - for cardiac arrhythmias (including arrhythmias caused by an overdose of cardiac glycosides)

Mode of application

Before use, you should consult your doctor. Orally, without chewing and with a sufficient amount of water. Panangin® Forte should be taken after meals, because the acidic environment of the stomach reduces its effectiveness. Recommended daily dose: 1 tablet 3 times/day. Maximum daily dose: 1 tablet 3 times/day.

Interaction

When used simultaneously with potassium-sparing diuretics (triamterene, spironolactone), beta-blockers, cyclosporine, heparin, ACE inhibitors, NSAIDs, the risk of developing hyperkalemia increases up to the appearance of arrhythmia and asystole. The use of potassium preparations together with GCS eliminates the hypokalemia they cause. Under the influence of potassium, observed reducing the undesirable effects of cardiac glycosides. Panangin® Forte enhances the negative dromo- and bathmotropic effects of antiarrhythmic drugs. Magnesium preparations reduce the effectiveness of neomycin, polymyxin B, tetracycline and streptomycin. Anesthetics enhance the inhibitory effect of magnesium preparations on the central nervous system. When used simultaneously with atracurium, dexamethonium, succinyl chloride and suxamethonium may enhance neuromuscular blockade. Calcitriol increases the concentration of magnesium in the blood plasma, calcium preparations reduce the effect of magnesium preparations. Pharmacokinetic interaction. Drugs with an astringent and enveloping effect reduce the absorption of potassium and magnesium aspraginate from the gastrointestinal tract, so it is necessary to observe 3- hour interval between oral administration of Panangin® Forte and the above medications.

Side effect

From the digestive system: possible nausea, vomiting, diarrhea, discomfort or burning sensation in the epigastric region (in patients with anacid gastritis or cholecystitis). From the cardiovascular system: possible AV blockade, paradoxical reaction (increased number of extrasystoles). aspects of water and electrolyte balance: hyperkalemia (nausea, vomiting, diarrhea, paresthesia), hypermagnesemia (facial redness, thirst, decreased blood pressure, hyporeflexia, respiratory depression, convulsions) are possible.

Contraindications

- hypersensitivity to the components of the drug; - acute and chronic renal failure; - hyperkalemia; - hypermagnesemia; - Addison's disease; - AV blockade of the I-III degree; - shock (including cardiogenic - AD Overdose. To date, cases of overdose have not been described. In case of overdose the risk of developing hyperkalemia and hypermagnesemia increases. Symptoms of hyperkalemia: increased fatigue, myasthenia gravis, paresthesia, confusion, heart rhythm disturbances (bradycardia, AV block, arrhythmias, cardiac arrest). Symptoms of hypermagnesemia: decreased neuromuscular excitability, nausea, vomiting, lethargy, decreased Blood pressure: With a sharp increase in the content of magnesium ions in the blood - inhibition of tendon reflexes, respiratory paralysis, coma.Treatment: discontinuation of the drug, symptomatic therapy (iv administration of 100 mg/min calcium chloride solution), if necessary, hemodialysis.

special instructions

Particular attention is required for patients with diseases accompanied by hyperkalemia: regular monitoring of potassium levels in the blood plasma is necessary. Impact on the ability to drive vehicles and machines. No studies have been conducted. No effect is expected on the ability to drive vehicles or operate mechanisms that require increased concentration and speed of psychomotor reactions.

Dispensing conditions in pharmacies

On prescription

Combination with other medications

The drug may enhance the negative effects of antiarrhythmic drugs. Panagin helps to cope with the lack of potassium ions in the blood, which is associated with prolonged use of diuretic medications. Non-steroidal anti-inflammatory drugs, heparin, cyclosporine, increase the likelihood of hyperkalemia. When using general anesthetics, the inhibitory effect of the drug on the central nervous system increases.

Increased neuromuscular blockade can occur under the influence of decamethonium, suxamethonium and atracuronium. The use of astringents and coating agents reduces the absorption of trace elements in the stomach.

The drug improves the tolerability of antiarrhythmic and cardiotonic drugs.

Instructions for use of Panangin drugs

Pharmacodynamics:

the most important intracellular cations of potassium (K+) and magnesium (Mg++) play a key role in the functioning of numerous enzymes, in the formation of bonds between macromolecules and intracellular structures and in the mechanism of muscle contractility.
The intra- and extracellular ratio of potassium, calcium, sodium and magnesium ions affects myocardial contractility. Endogenous aspartate acts as a conductor of ions: it has a high affinity for cells, due to the slight dissociation of its salts, ions in the form of complex compounds penetrate into the cells. Magnesium and potassium aspartates improve myocardial metabolism. Lack of magnesium/potassium predisposes to the development of arterial hypertension, atherosclerosis of the coronary arteries, arrhythmias and metabolic changes in the myocardium. Taking magnesium and potassium aspartates helps compensate for the lack of these electrolytes in food. Pharmacokinetics:
Magnesium

The total supply of magnesium in the body of a person weighing 70 kg is on average 24 g (1000 mmol); more than 60% of magnesium comes from bone tissue and about 40% from skeletal muscle and other tissues. About 1% of the total magnesium reserve in the body is found in the extracellular fluid, mainly in the blood serum. In healthy adults, the content of magnesium in the blood serum is in the range of 0.7-1.10 mmol/l. Magnesium is absorbed from the gastrointestinal tract by active transport. The main regulator of magnesium balance in the body is the kidneys. 3-5% of ionized magnesium is excreted by the kidneys. An increase in urine volume (for example, during loop diuretic therapy) leads to an increase in the excretion of ionized magnesium. If magnesium absorption in the small intestine is reduced, subsequent hypomagnesemia leads to a decrease in its excretion (less than 0.5 mmol/day).

Potassium

The total potassium reserve in the body of a person weighing 70 kg is on average 140 g (3570 mmol). The total potassium reserve is slightly less in women than in men and decreases slightly with age. 2% of the total potassium reserve in the body is located outside the cells, and the remaining 98% is inside the cells. Potassium is absorbed in the gastrointestinal tract. The optimal intake of potassium from food is 3-4 g (75-100 mmol) per day. The main route of potassium excretion is renal (about 90% of potassium is excreted by the kidneys daily). The remaining 10% is excreted through the gastrointestinal tract. Thus, the kidneys are responsible for long-term potassium homeostasis as well as plasma potassium levels. In the short term, blood potassium levels are also regulated by the flow of potassium between the intracellular and extracellular spaces.